Tumor necrosis factor alpha-mediated activation of c-Jun NH(2)-terminal kinase as a mechanism for fumonisin B(1) induced apoptosis in murine primary hepatocytes.

摘要: Fumonisin B(1) is a mycotoxin produced by Fusarium verticillioides, frequently associated with corn. It produces species-specific and organ-specific toxicity, including equine leukoencephalomalacia, porcine pulmonary edema, hepatic or renal damage in most animal species. perturbs sphingolipid metabolism inhibiting ceramide synthase. Our previous studies indicated that fumonisin caused localized activation of cytokines liver macrophages other cell types modulate induced apoptosis mice. The role tumor necrosis factor alpha (TNFalpha) mediated hepatocyte has been established; not much known about the downstream events leading to apoptosis. In current study, primary culture cells. consistence reports, accumulation sphingoid bases led increase TNFalpha expression. Phosphorylated total c-Jun NH(2)-terminal kinase (JNK) activities were increased after 24 h treatment. JNK inhibitor (SP600125) anti-TNFalpha reduced B(1). signaling production, as B(1)-mediated was presence medium, whereas did change Results this study imply generation results modulation mitogen activated protein kinases, particularly JNK, provides possible mechanism for murine hepatocytes.